High susceptibility to fatty liver disease in two-pore channel 2-deficient mice.

@article{Grimm2014HighST,
  title={High susceptibility to fatty liver disease in two-pore channel 2-deficient mice.},
  author={Christian Grimm and Lesca Miriam Holdt and Cheng-Chang Chen and Sami Abul Hassan and Christoph E. M{\"u}ller and Simone J{\"o}rs and Hartmut Cuny and Sandra Kissing and Bernd A Schr{\"o}der and Elisabeth S. Butz and Bernd H. Northoff and Jan Castonguay and Christian A. Luber and Markus Moser and Saskia Spahn and Renate L{\"u}llmann-Rauch and Christina Fendel and Norbert Klugbauer and Oliver Griesbeck and Albert Haas and Matthias Mann and Franz Bracher and Daniel Teupser and Paul Saftig and Martin Biel and Christian A. Wahl-Schott},
  journal={Nature communications},
  year={2014},
  volume={5},
  pages={4699}
}
Endolysosomal organelles play a key role in trafficking, breakdown and receptor-mediated recycling of different macromolecules such as low-density lipoprotein (LDL)-cholesterol, epithelial growth factor (EGF) or transferrin. Here we examine the role of two-pore channel (TPC) 2, an endolysosomal cation channel, in these processes. Embryonic mouse fibroblasts and hepatocytes lacking TPC2 display a profound impairment of LDL-cholesterol and EGF/EGF-receptor trafficking. Mechanistically, both… CONTINUE READING

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